Propionic acid affects immune status and metabolism in adipose tissue from overweight subjects

Eur J Clin Invest 2012; 42 (4): 357–364 Background  Adipose tissue is a primary site of obesity‐induced inflammation, which is emerging as an important contributor to obesity‐related diseases such as type 2 diabetes. Dietary fibre consumption appears to be protective. Short‐chain fatty acids, e.g. p...

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Published inEuropean journal of clinical investigation Vol. 42; no. 4; pp. 357 - 364
Main Authors Al-Lahham, Sa'ad, Roelofsen, Han, Rezaee, Farhad, Weening, Desiree, Hoek, Annemieke, Vonk, Roel, Venema, Koen
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.04.2012
Wiley-Blackwell
Subjects
Online AccessGet full text
ISSN0014-2972
1365-2362
1365-2362
DOI10.1111/j.1365-2362.2011.02590.x

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Abstract Eur J Clin Invest 2012; 42 (4): 357–364 Background  Adipose tissue is a primary site of obesity‐induced inflammation, which is emerging as an important contributor to obesity‐related diseases such as type 2 diabetes. Dietary fibre consumption appears to be protective. Short‐chain fatty acids, e.g. propionic acid, are the principal products of the colonic fermentation of dietary fibre and may have beneficial effects on adipose tissue inflammation. Materials and methods  Human omental adipose tissue explants were obtained from overweight (mean BMI 28·8) gynaecological patients who underwent surgery. Explants were incubated for 24 h with propionic acid. Human THP‐1 monocytic cells were differentiated to macrophages and incubated with LPS in the presence and absence of propionic acid. Cytokine and chemokine production were determined by multiplex‐ELISA, and mRNA expression of metabolic and macrophages genes was determined by RT‐PCR. Results  Treatment of adipose tissue explants with propionic acid results in a significant down‐regulation of several inflammatory cytokines and chemokines such as TNF‐α and CCL5. In addition, expression of lipoprotein lipase and GLUT4, associated with lipogenesis and glucose uptake, respectively, increased. Similar effects on cytokine and chemokine production by macrophages were observed. Conclusion  We show that propionic acid, normally produced in the colon, may have a direct beneficial effect on visceral adipose tissue, reducing obesity‐associated inflammation and increasing lipogenesis and glucose uptake. Effects on adipose tissue as a whole are at least partially explained by effects on macrophages but likely also adipocytes are involved. This suggests that, in vivo, propionic acid and dietary fibres may have potential in preventing obesity‐related inflammation and associated diseases.
AbstractList Adipose tissue is a primary site of obesity-induced inflammation, which is emerging as an important contributor to obesity-related diseases such as type 2 diabetes. Dietary fibre consumption appears to be protective. Short-chain fatty acids, e.g. propionic acid, are the principal products of the colonic fermentation of dietary fibre and may have beneficial effects on adipose tissue inflammation. Human omental adipose tissue explants were obtained from overweight (mean BMI 28·8) gynaecological patients who underwent surgery. Explants were incubated for 24 h with propionic acid. Human THP-1 monocytic cells were differentiated to macrophages and incubated with LPS in the presence and absence of propionic acid. Cytokine and chemokine production were determined by multiplex-ELISA, and mRNA expression of metabolic and macrophages genes was determined by RT-PCR. Treatment of adipose tissue explants with propionic acid results in a significant down-regulation of several inflammatory cytokines and chemokines such as TNF-α and CCL5. In addition, expression of lipoprotein lipase and GLUT4, associated with lipogenesis and glucose uptake, respectively, increased. Similar effects on cytokine and chemokine production by macrophages were observed. We show that propionic acid, normally produced in the colon, may have a direct beneficial effect on visceral adipose tissue, reducing obesity-associated inflammation and increasing lipogenesis and glucose uptake. Effects on adipose tissue as a whole are at least partially explained by effects on macrophages but likely also adipocytes are involved. This suggests that, in vivo, propionic acid and dietary fibres may have potential in preventing obesity-related inflammation and associated diseases.
Eur J Clin Invest 2012; 42 (4): 357–364 Background  Adipose tissue is a primary site of obesity‐induced inflammation, which is emerging as an important contributor to obesity‐related diseases such as type 2 diabetes. Dietary fibre consumption appears to be protective. Short‐chain fatty acids, e.g. propionic acid, are the principal products of the colonic fermentation of dietary fibre and may have beneficial effects on adipose tissue inflammation. Materials and methods  Human omental adipose tissue explants were obtained from overweight (mean BMI 28·8) gynaecological patients who underwent surgery. Explants were incubated for 24 h with propionic acid. Human THP‐1 monocytic cells were differentiated to macrophages and incubated with LPS in the presence and absence of propionic acid. Cytokine and chemokine production were determined by multiplex‐ELISA, and mRNA expression of metabolic and macrophages genes was determined by RT‐PCR. Results  Treatment of adipose tissue explants with propionic acid results in a significant down‐regulation of several inflammatory cytokines and chemokines such as TNF‐α and CCL5. In addition, expression of lipoprotein lipase and GLUT4, associated with lipogenesis and glucose uptake, respectively, increased. Similar effects on cytokine and chemokine production by macrophages were observed. Conclusion  We show that propionic acid, normally produced in the colon, may have a direct beneficial effect on visceral adipose tissue, reducing obesity‐associated inflammation and increasing lipogenesis and glucose uptake. Effects on adipose tissue as a whole are at least partially explained by effects on macrophages but likely also adipocytes are involved. This suggests that, in vivo, propionic acid and dietary fibres may have potential in preventing obesity‐related inflammation and associated diseases.
Background Adipose tissue is a primary site of obesity-induced inflammation, which is emerging as an important contributor to obesity-related diseases such as type 2 diabetes. Dietary fibre consumption appears to be protective. Short-chain fatty acids, e.g. propionic acid, are the principal products of the colonic fermentation of dietary fibre and may have beneficial effects on adipose tissue inflammation. Materials and methods Human omental adipose tissue explants were obtained from overweight (mean BMI 28.8) gynaecological patients who underwent surgery. Explants were incubated for 24h with propionic acid. Human THP-1 monocytic cells were differentiated to macrophages and incubated with LPS in the presence and absence of propionic acid. Cytokine and chemokine production were determined by multiplex-ELISA, and mRNA expression of metabolic and macrophages genes was determined by RT-PCR. Results Treatment of adipose tissue explants with propionic acid results in a significant down-regulation of several inflammatory cytokines and chemokines such as TNF- alpha and CCL5. In addition, expression of lipoprotein lipase and GLUT4, associated with lipogenesis and glucose uptake, respectively, increased. Similar effects on cytokine and chemokine production by macrophages were observed. Conclusion We show that propionic acid, normally produced in the colon, may have a direct beneficial effect on visceral adipose tissue, reducing obesity-associated inflammation and increasing lipogenesis and glucose uptake. Effects on adipose tissue as a whole are at least partially explained by effects on macrophages but likely also adipocytes are involved. This suggests that, in vivo, propionic acid and dietary fibres may have potential in preventing obesity-related inflammation and associated diseases.Original Abstract: Eur J Clin Invest 2012; 42 (4): 357-364
Adipose tissue is a primary site of obesity-induced inflammation, which is emerging as an important contributor to obesity-related diseases such as type 2 diabetes. Dietary fibre consumption appears to be protective. Short-chain fatty acids, e.g. propionic acid, are the principal products of the colonic fermentation of dietary fibre and may have beneficial effects on adipose tissue inflammation.BACKGROUNDAdipose tissue is a primary site of obesity-induced inflammation, which is emerging as an important contributor to obesity-related diseases such as type 2 diabetes. Dietary fibre consumption appears to be protective. Short-chain fatty acids, e.g. propionic acid, are the principal products of the colonic fermentation of dietary fibre and may have beneficial effects on adipose tissue inflammation.Human omental adipose tissue explants were obtained from overweight (mean BMI 28·8) gynaecological patients who underwent surgery. Explants were incubated for 24 h with propionic acid. Human THP-1 monocytic cells were differentiated to macrophages and incubated with LPS in the presence and absence of propionic acid. Cytokine and chemokine production were determined by multiplex-ELISA, and mRNA expression of metabolic and macrophages genes was determined by RT-PCR.MATERIALS AND METHODSHuman omental adipose tissue explants were obtained from overweight (mean BMI 28·8) gynaecological patients who underwent surgery. Explants were incubated for 24 h with propionic acid. Human THP-1 monocytic cells were differentiated to macrophages and incubated with LPS in the presence and absence of propionic acid. Cytokine and chemokine production were determined by multiplex-ELISA, and mRNA expression of metabolic and macrophages genes was determined by RT-PCR.Treatment of adipose tissue explants with propionic acid results in a significant down-regulation of several inflammatory cytokines and chemokines such as TNF-α and CCL5. In addition, expression of lipoprotein lipase and GLUT4, associated with lipogenesis and glucose uptake, respectively, increased. Similar effects on cytokine and chemokine production by macrophages were observed.RESULTSTreatment of adipose tissue explants with propionic acid results in a significant down-regulation of several inflammatory cytokines and chemokines such as TNF-α and CCL5. In addition, expression of lipoprotein lipase and GLUT4, associated with lipogenesis and glucose uptake, respectively, increased. Similar effects on cytokine and chemokine production by macrophages were observed.We show that propionic acid, normally produced in the colon, may have a direct beneficial effect on visceral adipose tissue, reducing obesity-associated inflammation and increasing lipogenesis and glucose uptake. Effects on adipose tissue as a whole are at least partially explained by effects on macrophages but likely also adipocytes are involved. This suggests that, in vivo, propionic acid and dietary fibres may have potential in preventing obesity-related inflammation and associated diseases.CONCLUSIONWe show that propionic acid, normally produced in the colon, may have a direct beneficial effect on visceral adipose tissue, reducing obesity-associated inflammation and increasing lipogenesis and glucose uptake. Effects on adipose tissue as a whole are at least partially explained by effects on macrophages but likely also adipocytes are involved. This suggests that, in vivo, propionic acid and dietary fibres may have potential in preventing obesity-related inflammation and associated diseases.
Author Al-Lahham, Sa'ad
Rezaee, Farhad
Weening, Desiree
Roelofsen, Han
Venema, Koen
Hoek, Annemieke
Vonk, Roel
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  givenname: Sa'ad
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  givenname: Han
  surname: Roelofsen
  fullname: Roelofsen, Han
  organization: Centre for Medical Biomics, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
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  givenname: Farhad
  surname: Rezaee
  fullname: Rezaee, Farhad
  organization: Centre for Medical Biomics, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
– sequence: 4
  givenname: Desiree
  surname: Weening
  fullname: Weening, Desiree
  organization: Centre for Medical Biomics, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
– sequence: 5
  givenname: Annemieke
  surname: Hoek
  fullname: Hoek, Annemieke
  organization: Department of Obstetrics and Gynecology, University Medical Centre Groningen, Groningen, The Netherlands
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  surname: Vonk
  fullname: Vonk, Roel
  organization: Centre for Medical Biomics, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands
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  givenname: Koen
  surname: Venema
  fullname: Venema, Koen
  organization: Top Institute Food and Nutrition, Wageningen, The Netherlands
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Issue 4
Keywords Human
Short chain
Adipose tissue
Nutrition
Propionic acid
Body weight
Lipids
Corporal biometry
Inflammation
Metabolism
Fatty acids
Immunity
Feeding
Overweight
Medicine
Diet therapy
Diet
dietary fibre
short-chain fatty acids
Food
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
CC BY 4.0
2011 The Authors. European Journal of Clinical Investigation © 2011 Stichting European Society for Clinical Investigation Journal Foundation.
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References Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J Clin Invest 2005;115:1111-9.
Cani PD, Knauf C, Iglesias MA, Drucker DJ, Delzenne NM, Burcelin R. Improvement of glucose tolerance and hepatic insulin sensitivity by oligofructose requires a functional glucagon-like peptide 1 receptor. Diabetes 2006;55:1484-90.
Bloemen JG, Venema K, van de Poll MC, Olde Damink SW, Buurman WA, Dejong CH. Short chain fatty acids exchange across the gut and liver in humans measured at surgery. Clin Nutr 2009;28:657-61.
Delzenne NM, Daubioul C, Neyrinck A, Lasa M, Taper HS. Insulin and oligofructose modulate lipid metabolism in animals: review of biochemical events and future prospects. Br J Nutr 2002;87(Suppl. 2):S255-9.
Lyra A, Lahtinen S, Tiihonen K, Ouwehand AC. Intestinal microbiota and overweight. Benef Microbes 2010;1:407-21.
Howarth NC, Saltzman E, Roberts SB. Dietary fiber and weight regulation. Nutr Rev 2001;59:129-39.
van Eijk HM, Bloemen JG, Dejong CH. Application of liquid chromatography-mass spectrometry to measure short chain fatty acids in blood. J Chromatogr B Analyt Technol Biomed Life Sci 2009;877:719-24.
Al-Lahham SH, Peppelenbosch MP, Roelofsen H, Vonk RJ, Venema K. Biological effects of propionic acid in humans; metabolism, potential applications and underlying mechanisms. Biochim Biophys Acta 2010;1801:1175-83.
Place RF, Noonan EJ, Giardina C. HDAC inhibition prevents NF-kappa B activation by suppressing proteasome activity: down-regulation of proteasome subunit expression stabilizes I kappa B alpha. Biochem Pharmacol 2005;70:394-406.
Toeller M. Fibre consumption, metabolic effects and prevention of complications in diabetic patients: epidemiological evidence. Dig Liver Dis 2002;34(Suppl. 2):S145-9.
Galisteo M, Duarte J, Zarzuelo A. Effects of dietary fibers on disturbances clustered in the metabolic syndrome. J Nutr Biochem 2008;19:71-84.
Wong JM, de Souza R, Kendall CW, Emam A, Jenkins DJ. Colonic health: fermentation and short chain fatty acids. J Clin Gastroenterol 2006;40:235-43.
Cummings JH, Pomare EW, Branch WJ, Naylor CP, Macfarlane GT. Short chain fatty acids in human large intestine, portal, hepatic and venous blood. Gut 1987;28:1221-7.
Meijer K, de Vos P, Priebe MG. Butyrate and other short-chain fatty acids as modulators of immunity: what relevance for health? Curr Opin Clin Nutr Metab Care 2010;13:715-21.
Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005;352:1685-95.
Festa A, D'Agostino R Jr, Williams K, Karter AJ, Mayer-Davis EJ, Tracy RP et al. The relation of body fat mass and distribution to markers of chronic inflammation. Int J Obes Relat Metab Disord 2001;25:1407-15.
Tedelind S, Westberg F, Kjerrulf M, Vidal A. Anti-inflammatory properties of the short-chain fatty acids acetate and propionate: a study with relevance to inflammatory bowel disease. World J Gastroenterol 2007;13:2826-32.
Peters SG, Pomare EW, Fisher CA. Portal and peripheral blood short chain fatty acid concentrations after caecal lactulose instillation at surgery. Gut 1992;33:1249-52.
Tappenden KA, Thomson AB, Wild GE, McBurney MI. Short-chain fatty acids increase proglucagon and ornithine decarboxylase messenger RNAs after intestinal resection in rats. JPEN J Parenter Enteral Nutr 1996;20:357-62.
Kusminski CM, da Silva NF, Creely SJ, Fisher FM, Harte AL, Baker AR et al. The in vitro effects of resistin on the innate immune signaling pathway in isolated human subcutaneous adipocytes. J Clin Endocrinol Metab 2007;92:270-6.
Van Gaal LF, Mertens IL, De Block CE. Mechanisms linking obesity with cardiovascular disease. Nature 2006;444:875-80.
Dankert J, Zijlstra JB, Wolthers BG. Volatile fatty acids in human peripheral and portal blood: quantitative determination vacuum distillation and gas chromatography. Clin Chim Acta 1981;110:301-7.
Maslowski KM, Vieira AT, Ng A, Kranich J, Sierro F, Yu D et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43. Nature 2009;461:1282-6.
Venema K. Role of gut microbiota in the control of energy and carbohydrate metabolism. Curr Opin Clin Nutr Metab Care 2010;13:432-8.
Keenan MJ, Zhou J, McCutcheon KL, Raggio AM, Bateman HG, Todd E et al. Effects of resistant starch, a non-digestible fermentable fiber, on reducing body fat. Obesity (Silver Spring) 2006;14:1523-34.
Ferchaud-Roucher V, Pouteau E, Piloquet H, Zair Y, Krempf M. Colonic fermentation from lactulose inhibits lipolysis in overweight subjects. Am J Physiol Endocrinol Metab 2005;289:E716-20.
Al-Lahham SH, Roelofsen H, Priebe M, Weening D, Dijkstra M, Hoek A et al. Regulation of adipokine production in human adipose tissue by propionic acid. Eur J Clin Invest 2010;40:401-7.
Kamei N, Tobe K, Suzuki R, Ohsugi M, Watanabe T, Kubota N et al. Overexpression of monocyte chemoattractant protein-1 in adipose tissues causes macrophage recruitment and insulin resistance. J Biol Chem 2006;281:26602-14.
Vandesompele J, De Preter K, Pattyn F, Poppe B, Van Roy N, De Paepe A et al. Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes. Genome Biol 2002;3, RESEARCH0034.
Im SS, Kwon SK, Kang SY, Kim TH, Kim HI, Hur MW et al. Regulation of GLUT4 gene expression by SREBP-1c in adipocytes. Biochem J 2006;399:131-9.
Kanda H, Tateya S, Tamori Y, Kotani K, Hiasa K, Kitazawa R et al. MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. J Clin Invest 2006;116:1494-505.
Roelofsen H, Priebe MG, Vonk RJ. The interaction of short-chain fatty acids with adipose tissue: relevance for prevention of type 2 diabetes. Benef Microbes 2010;1:433-7.
Cummings JH, Gibson GR, Macfarlane GT. Quantitative estimates of fermentation in the hind gut of man. Acta Vet Scand Suppl 1989;86:76-82.
Meijer K, de Vries M, Al-Lahham S, Bruinenberg M, Weening D, Dijkstra M et al. Human primary adipocytes exhibit immune cell function: adipocytes prime inflammation independent of macrophages. PLoS ONE 2011;6:e17154.
Brown AJ, Goldsworthy SM, Barnes AA, Eilert MM, Tcheang L, Daniels D et al. The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. J Biol Chem 2003;278:11312-9.
Juge-Aubry CE, Henrichot E, Meier CA. Adipose tissue: a regulator of inflammation. Best Pract Res Clin Endocrinol Metab 2005;19:547-66.
Kim JB, Spiegelman BM. ADD1/SREBP1 promotes adipocyte differentiation and gene expression linked to fatty acid metabolism. Genes Dev 1996;10:1096-107.
Cani PD, Joly E, Horsmans Y, Delzenne NM. Oligofructose promotes satiety in healthy human: a pilot study. Eur J Clin Nutr 2006;60:567-72.
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References_xml – reference: Kusminski CM, da Silva NF, Creely SJ, Fisher FM, Harte AL, Baker AR et al. The in vitro effects of resistin on the innate immune signaling pathway in isolated human subcutaneous adipocytes. J Clin Endocrinol Metab 2007;92:270-6.
– reference: Van Gaal LF, Mertens IL, De Block CE. Mechanisms linking obesity with cardiovascular disease. Nature 2006;444:875-80.
– reference: Tedelind S, Westberg F, Kjerrulf M, Vidal A. Anti-inflammatory properties of the short-chain fatty acids acetate and propionate: a study with relevance to inflammatory bowel disease. World J Gastroenterol 2007;13:2826-32.
– reference: Maslowski KM, Vieira AT, Ng A, Kranich J, Sierro F, Yu D et al. Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43. Nature 2009;461:1282-6.
– reference: Bloemen JG, Venema K, van de Poll MC, Olde Damink SW, Buurman WA, Dejong CH. Short chain fatty acids exchange across the gut and liver in humans measured at surgery. Clin Nutr 2009;28:657-61.
– reference: Juge-Aubry CE, Henrichot E, Meier CA. Adipose tissue: a regulator of inflammation. Best Pract Res Clin Endocrinol Metab 2005;19:547-66.
– reference: Delzenne NM, Daubioul C, Neyrinck A, Lasa M, Taper HS. Insulin and oligofructose modulate lipid metabolism in animals: review of biochemical events and future prospects. Br J Nutr 2002;87(Suppl. 2):S255-9.
– reference: Lyra A, Lahtinen S, Tiihonen K, Ouwehand AC. Intestinal microbiota and overweight. Benef Microbes 2010;1:407-21.
– reference: Brown AJ, Goldsworthy SM, Barnes AA, Eilert MM, Tcheang L, Daniels D et al. The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acids. J Biol Chem 2003;278:11312-9.
– reference: Place RF, Noonan EJ, Giardina C. HDAC inhibition prevents NF-kappa B activation by suppressing proteasome activity: down-regulation of proteasome subunit expression stabilizes I kappa B alpha. Biochem Pharmacol 2005;70:394-406.
– reference: Festa A, D'Agostino R Jr, Williams K, Karter AJ, Mayer-Davis EJ, Tracy RP et al. The relation of body fat mass and distribution to markers of chronic inflammation. Int J Obes Relat Metab Disord 2001;25:1407-15.
– reference: Tappenden KA, Thomson AB, Wild GE, McBurney MI. Short-chain fatty acids increase proglucagon and ornithine decarboxylase messenger RNAs after intestinal resection in rats. JPEN J Parenter Enteral Nutr 1996;20:357-62.
– reference: Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J Clin Invest 2005;115:1111-9.
– reference: Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med 2005;352:1685-95.
– reference: Roelofsen H, Priebe MG, Vonk RJ. The interaction of short-chain fatty acids with adipose tissue: relevance for prevention of type 2 diabetes. Benef Microbes 2010;1:433-7.
– reference: Dankert J, Zijlstra JB, Wolthers BG. Volatile fatty acids in human peripheral and portal blood: quantitative determination vacuum distillation and gas chromatography. Clin Chim Acta 1981;110:301-7.
– reference: Cani PD, Knauf C, Iglesias MA, Drucker DJ, Delzenne NM, Burcelin R. Improvement of glucose tolerance and hepatic insulin sensitivity by oligofructose requires a functional glucagon-like peptide 1 receptor. Diabetes 2006;55:1484-90.
– reference: Kamei N, Tobe K, Suzuki R, Ohsugi M, Watanabe T, Kubota N et al. Overexpression of monocyte chemoattractant protein-1 in adipose tissues causes macrophage recruitment and insulin resistance. J Biol Chem 2006;281:26602-14.
– reference: Cummings JH, Pomare EW, Branch WJ, Naylor CP, Macfarlane GT. Short chain fatty acids in human large intestine, portal, hepatic and venous blood. Gut 1987;28:1221-7.
– reference: Cani PD, Joly E, Horsmans Y, Delzenne NM. Oligofructose promotes satiety in healthy human: a pilot study. Eur J Clin Nutr 2006;60:567-72.
– reference: Galisteo M, Duarte J, Zarzuelo A. Effects of dietary fibers on disturbances clustered in the metabolic syndrome. J Nutr Biochem 2008;19:71-84.
– reference: Keenan MJ, Zhou J, McCutcheon KL, Raggio AM, Bateman HG, Todd E et al. Effects of resistant starch, a non-digestible fermentable fiber, on reducing body fat. Obesity (Silver Spring) 2006;14:1523-34.
– reference: Peters SG, Pomare EW, Fisher CA. Portal and peripheral blood short chain fatty acid concentrations after caecal lactulose instillation at surgery. Gut 1992;33:1249-52.
– reference: Meijer K, de Vries M, Al-Lahham S, Bruinenberg M, Weening D, Dijkstra M et al. Human primary adipocytes exhibit immune cell function: adipocytes prime inflammation independent of macrophages. PLoS ONE 2011;6:e17154.
– reference: Toeller M. Fibre consumption, metabolic effects and prevention of complications in diabetic patients: epidemiological evidence. Dig Liver Dis 2002;34(Suppl. 2):S145-9.
– reference: Howarth NC, Saltzman E, Roberts SB. Dietary fiber and weight regulation. Nutr Rev 2001;59:129-39.
– reference: Meijer K, de Vos P, Priebe MG. Butyrate and other short-chain fatty acids as modulators of immunity: what relevance for health? Curr Opin Clin Nutr Metab Care 2010;13:715-21.
– reference: Wong JM, de Souza R, Kendall CW, Emam A, Jenkins DJ. Colonic health: fermentation and short chain fatty acids. J Clin Gastroenterol 2006;40:235-43.
– reference: Ferchaud-Roucher V, Pouteau E, Piloquet H, Zair Y, Krempf M. Colonic fermentation from lactulose inhibits lipolysis in overweight subjects. Am J Physiol Endocrinol Metab 2005;289:E716-20.
– reference: Kim JB, Spiegelman BM. ADD1/SREBP1 promotes adipocyte differentiation and gene expression linked to fatty acid metabolism. Genes Dev 1996;10:1096-107.
– reference: Cummings JH, Gibson GR, Macfarlane GT. Quantitative estimates of fermentation in the hind gut of man. Acta Vet Scand Suppl 1989;86:76-82.
– reference: van Eijk HM, Bloemen JG, Dejong CH. Application of liquid chromatography-mass spectrometry to measure short chain fatty acids in blood. J Chromatogr B Analyt Technol Biomed Life Sci 2009;877:719-24.
– reference: Venema K. Role of gut microbiota in the control of energy and carbohydrate metabolism. Curr Opin Clin Nutr Metab Care 2010;13:432-8.
– reference: Kanda H, Tateya S, Tamori Y, Kotani K, Hiasa K, Kitazawa R et al. MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. J Clin Invest 2006;116:1494-505.
– reference: Al-Lahham SH, Roelofsen H, Priebe M, Weening D, Dijkstra M, Hoek A et al. Regulation of adipokine production in human adipose tissue by propionic acid. Eur J Clin Invest 2010;40:401-7.
– reference: Im SS, Kwon SK, Kang SY, Kim TH, Kim HI, Hur MW et al. Regulation of GLUT4 gene expression by SREBP-1c in adipocytes. Biochem J 2006;399:131-9.
– reference: Vandesompele J, De Preter K, Pattyn F, Poppe B, Van Roy N, De Paepe A et al. Accurate normalization of real-time quantitative RT-PCR data by geometric averaging of multiple internal control genes. Genome Biol 2002;3, RESEARCH0034.
– reference: Al-Lahham SH, Peppelenbosch MP, Roelofsen H, Vonk RJ, Venema K. Biological effects of propionic acid in humans; metabolism, potential applications and underlying mechanisms. Biochim Biophys Acta 2010;1801:1175-83.
– volume: 115
  start-page: 1111
  year: 2005
  end-page: 9
  article-title: Inflammation, stress, and diabetes
  publication-title: J Clin Invest
– volume: 34
  start-page: S145
  issue: Suppl. 2
  year: 2002
  end-page: 9
  article-title: Fibre consumption, metabolic effects and prevention of complications in diabetic patients: epidemiological evidence
  publication-title: Dig Liver Dis
– volume: 461
  start-page: 1282
  year: 2009
  end-page: 6
  article-title: Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43
  publication-title: Nature
– volume: 281
  start-page: 26602
  year: 2006
  end-page: 14
  article-title: Overexpression of monocyte chemoattractant protein‐1 in adipose tissues causes macrophage recruitment and insulin resistance
  publication-title: J Biol Chem
– volume: 3
  year: 2002
  article-title: Accurate normalization of real‐time quantitative RT‐PCR data by geometric averaging of multiple internal control genes
  publication-title: Genome Biol
– volume: 55
  start-page: 1484
  year: 2006
  end-page: 90
  article-title: Improvement of glucose tolerance and hepatic insulin sensitivity by oligofructose requires a functional glucagon‐like peptide 1 receptor
  publication-title: Diabetes
– volume: 28
  start-page: 1221
  year: 1987
  end-page: 7
  article-title: Short chain fatty acids in human large intestine, portal, hepatic and venous blood
  publication-title: Gut
– volume: 33
  start-page: 1249
  year: 1992
  end-page: 52
  article-title: Portal and peripheral blood short chain fatty acid concentrations after caecal lactulose instillation at surgery
  publication-title: Gut
– volume: 70
  start-page: 394
  year: 2005
  end-page: 406
  article-title: HDAC inhibition prevents NF‐kappa B activation by suppressing proteasome activity: down‐regulation of proteasome subunit expression stabilizes I kappa B alpha
  publication-title: Biochem Pharmacol
– volume: 19
  start-page: 547
  year: 2005
  end-page: 66
  article-title: Adipose tissue: a regulator of inflammation
  publication-title: Best Pract Res Clin Endocrinol Metab
– volume: 352
  start-page: 1685
  year: 2005
  end-page: 95
  article-title: Inflammation, atherosclerosis, and coronary artery disease
  publication-title: N Engl J Med
– volume: 289
  start-page: E716
  year: 2005
  end-page: 20
  article-title: Colonic fermentation from lactulose inhibits lipolysis in overweight subjects
  publication-title: Am J Physiol Endocrinol Metab
– volume: 59
  start-page: 129
  year: 2001
  end-page: 39
  article-title: Dietary fiber and weight regulation
  publication-title: Nutr Rev
– start-page: 17
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– volume: 13
  start-page: 715
  year: 2010
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  article-title: Butyrate and other short‐chain fatty acids as modulators of immunity: what relevance for health?
  publication-title: Curr Opin Clin Nutr Metab Care
– volume: 6
  start-page: e17154
  year: 2011
  article-title: Human primary adipocytes exhibit immune cell function: adipocytes prime inflammation independent of macrophages
  publication-title: PLoS ONE
– volume: 92
  start-page: 270
  year: 2007
  end-page: 6
  article-title: The in vitro effects of resistin on the innate immune signaling pathway in isolated human subcutaneous adipocytes
  publication-title: J Clin Endocrinol Metab
– volume: 110
  start-page: 301
  year: 1981
  end-page: 7
  article-title: Volatile fatty acids in human peripheral and portal blood: quantitative determination vacuum distillation and gas chromatography
  publication-title: Clin Chim Acta
– volume: 14
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  year: 2006
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Snippet Eur J Clin Invest 2012; 42 (4): 357–364 Background  Adipose tissue is a primary site of obesity‐induced inflammation, which is emerging as an important...
Adipose tissue is a primary site of obesity-induced inflammation, which is emerging as an important contributor to obesity-related diseases such as type 2...
Background Adipose tissue is a primary site of obesity-induced inflammation, which is emerging as an important contributor to obesity-related diseases such as...
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StartPage 357
SubjectTerms Adipocytes
Adipose tissue
Adipose Tissue - drug effects
Adipose Tissue - immunology
Adipose Tissue - metabolism
Biological and medical sciences
Body weight
Cells, Cultured - metabolism
Chemokines
Colon
Cytokines
Cytokines - genetics
Cytokines - metabolism
Diabetes mellitus
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - metabolism
Dietary fiber
dietary fibre
Diseases of the digestive system
Enzyme-Linked Immunosorbent Assay
Explants
Fatty acids
Female
Fermentation
Gene expression
General aspects
Glucose
Glucose Transporter Type 4 - metabolism
Humans
Immune status
Inflammation
Lipogenesis
Lipopolysaccharides
Lipoprotein lipase
Lipoprotein Lipase - metabolism
Macrophages
Macrophages - immunology
Medical sciences
Metabolic diseases
Metabolism
Monocytes
Obesity
Omentum - metabolism
Overweight - immunology
Polymerase chain reaction
Propionates - pharmacology
Propionic acid
Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
short-chain fatty acids
Surgery
Tumor necrosis factor- alpha
Title Propionic acid affects immune status and metabolism in adipose tissue from overweight subjects
URI https://api.istex.fr/ark:/67375/WNG-CRH2956Q-R/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1365-2362.2011.02590.x
https://www.ncbi.nlm.nih.gov/pubmed/21913915
https://www.proquest.com/docview/1020845910
https://www.proquest.com/docview/928908466
Volume 42
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